CASE 10928 Published on 16.05.2013
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Non-alcoholic Wernicke’s encephalopathy- Role of MRI in diagnosis and follow up

Section

Neuroradiology

Case Type

Clinical Cases

Authors

Sandeep M B, Omprakash A R, Subas Chandra, Ram shenoy Basti

Department of Radiodiagnosis,
Father muller medical college.
Mangalore, India.
Connected authors
Patient

27 years, female

Categories
Area of Interest Neuroradiology brain ; Imaging Technique MR
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Clinical History
A 27-year-old woman came with bilious vomiting and abdominal pain for the past 4 days and two episodes of abnormal movements of hands and feet associated with uprolling of eyes and tongue bite followed by altered behaviour. She was conscious, oriented, with hypotonia and absent power in all four limbs.
Imaging Findings
Symmetrical T2 and FLAIR hyperintensities in the hypothalamus, medial thalami, periaqueductal grey matter, mammilary bodies, lateral walls of the 3rd ventricle and bilateral frontal gyri. There were few focal bright areas in diffusion weighted study involving bifrontal cortex. No significant post-contrast enhancement seen in these lesions.
Post treatment follow up MR imaging was done after 15 days which showed significant reduction of the T2 and FLAIR hyperintensities.
Discussion
Wernicke’s encephalopathy is a medical emergency which occurs due to acute deficiency of thiamine and presents with neuropsychatric manifestations [1].
Wernicke’s encephalopathy is an eponymical disease named after Dr Carl Wernicke who described the classical triad of its clinical manifestation consisting of ocular signs, altered consciousness, and ataxia [2].
The classical clinical triad of Wernicke’s encephalopathy described by Dr Carl is present only in 10 % of the presenting cases [3].
Imbalance of thiamine, the body stores of which take approximately 6 weeks to get exhausted, induces various biochemical and metabolic changes [4].
The clinical manifestations of the disease also include loss of appetite, nausea and vomiting, fatigue, apathy, giddiness, insomnia, anxiety, amnesia for immediate past, confusion, disorientation, hallucinations and even coma [5].
Chronic alcohol abuse is the most common cause of Wernicke’s encephalopathy [6] however, few cases of non-alcoholic Wernicke’s encephalopathy have also been reported [7, 8].
The manifestations of Wernicke’s encephalopathy can occur with normal circulating thiamine levels as most of thiamine is in the stored form and is used in glucose metabolism [9].
MRI is a sensitive tool in diagnosing Wernicke’s encephalopathy. Oedema of cytotoxic and vasogenic origin is the most characteristic neuroimaging finding of acute Wernicke encephalopathy [10].
In acute Wernicke’s encephalopathy symmetric involvement of brain is noted, typical findings being increased T2 and decreased T1 signal surrounding the aqueduct and third ventricle, medial thalamus, the tectal plate, periaqueductal gray matter and mamillary bodies [11].
The atypical findings of Wernicke’s encephalopathy are symmetrical distribution of hyperintense lesions in cerebellar dentate nuclei, tegmentum of the lower pons, red nuclei, and tectum of the midbrain [12, 13].
Contrast enhancement can be present in the lesions, frequently in the mamillary bodies which is more often seen in alcoholic patients. Enhancing mamillary bodies can sometimes be the only sign of Wernicke's encephalopathy [7]. Gadolinium enhanced studies are hence advocated in this condition.
In Wernicke's encephalopathy, involvement of the cortex on imaging is rare and this finding if present carries a poor prognosis [14].
Patients in whom Wernicke's encephalopathy is suspected, thiamine should be initiated either intravenously or intramuscularly as early as possible to ensure adequate absorption [15].
The MRI findings revert following treatment with thiamine [16].
This is a medical emergency and requires early diagnosis and treatment. Failure to diagnose and initiate adequate treatment at the correct time in the form of parenteral therapy may even cause loss of life in 20% of cases; 75% will be left with permanent brain damage known as the Korsakoff's Psychosis [17].
Differential Diagnosis List
Non-alcoholic Wernicke’s encephalopathy
Artery of percheron infarct
Metronidazole induced encephalopathy
Creudztfeldt-Jacob disease.
Deep cerebral venous thrombosis
Final Diagnosis
Non-alcoholic Wernicke’s encephalopathy
Case information
URL: https://www.eurorad.org/case/10928
DOI: 10.1594/EURORAD/CASE.10928
ISSN: 1563-4086
Figure 1

MRI Brain FLAIR images

MRI Brain FLAIR images
MRI FLAIR sequence axial section at the level of midbrain showing hyperintensity in the peri aqueductal grey matter and bilateral mamillary bodies.
MRI Brain FLAIR images
MRI FLAIR sequence axial section at the level of thalamus showing hyperintensity in the medial thalami and lateral walls of the third ventricle
MRI Brain FLAIR images
MRI FLAIR sequence axial section at the supraventricular level showing hyperintensity in the bilateral frontal gyri
Figure 2

MRI brain T2W images

MRI brain T2W images
MRI T2W sequence axial section at the level of mid brain showing hyperintensity in periaqueductal grey matter
MRI brain T2W images
MRI T2W sequence axial section at the level of thalamus showing hyperintensity in the medial thalami and lateral walls of the third ventricle
MRI brain T2W images
MRI T2W sequence axial section at the supraventricular level showing hyperintensity in the bilateral frontal gyri
Figure 3

MRI Brain DW image

MRI Brain DW image
MRI DW sequence axial section at the supraventricular level showing restriction at the bilateral frontal gyri
Figure 4

MRI Brain T1 Contrast enhanced images

MRI Brain T1 Contrast enhanced images
MRI T1 contrast enhanced axial section at the level of midbrain showing no evidence of abnormal contrast enhancement
MRI Brain T1 Contrast enhanced images
MRI T1 contrast enhanced axial section at the level of thalamus showing no evidence of abnormal contrast enhancement
Figure 5

MRI Brain post treatment images

MRI Brain post treatment images
MRI FLAIR sequence axial section at the level of midbrain showing significant reduction of hyperintensity in the peri aqueductal grey matter
MRI Brain post treatment images
MRI FLAIR sequence axial section at the level of thalamus showing significant reduction of hyperintensity in the bilateral thalami and lateral walls of third ventricle
MRI Brain post treatment images
MRI T2 sequence axial section at the level of thalamus showing significant reduction of hyperintensity in the bilateral thalami and lateral walls of third ventricle